Lactate Gap Research Articles

Suggested guide to using lactate gap as a surrogate marker in the diagnosis of ethylene glycol overdose.

Ethylene glycol (EG) poisoning, if not diagnosed rapidly, can lead to poor patient outcomes. Gas Chromatography (GC) is primarily used for EG quantitation which is rarely available, and the turn-around time may be prolonged. Most lactate results from point-of care (POCT) methods are falsely elevated in EG poisoning compared with automated chemistry analyser results. In combination the lactate gap (POCT-Automated chemistry) can be used as surrogate marker in just about all laboratories to indicate likely EG toxicity and guide treatment. A male presented by ambulance to hospital with severe agitation requiring mechanical ventilation to facilitate ongoing management. Venous blood gas analysis confirmed a high anion gap metabolic acidosis (HAGMA) with an elevated lactate. The lactate and osmolarity measured in the laboratory showed a normal lactate and high osmolarity, giving a large osmolar gap. The patient was immediately commenced on renal replacement therapy for presumed EG poisoning to minimize kidney injury, and the treatment continued for 19 hours. A very high EG concentration was confirmed by GC the next day. An elevated lactate gap along with a HAGMA and osmolar gap can provide rapid surrogate laboratory data indicating EG poisoning enabling timely treatment and better patient outcomes.

Lactate Gap: A Diagnostic Clue for Diagnosing and Managing Ethylene Glycol Poisoning

Lactate Gap: A Diagnostic Clue for Diagnosing and Managing Ethylene Glycol Poisoning

A False-Positive Gamma-Hydroxy Butyric Acid Urine Screening in a Patient with High Anion Gap Metabolic Acidosis Due to Ethylene Glycol Poisoning.

A young woman with a history of several suicide attempts was admitted to the hospital after suspicion of a new intoxication without definite identification of the causing agent. The patient had a high anion gap metabolic acidosis (HAGMA) with respiratory compensation, a lactate gap and an osmolar gap at admission. Initial toxicological screening showed no abnormalities except for a weak positive gamma-hydroxy butyric acid (GHB) enzymatic screen in urine. This finding could not be confirmed using chromatographic analysis nor be explained by the presence of known cross-reacting substances like ethanol. In this case, falsely elevated urinary GHB screening was caused by the ingestion of ethylene glycol. To confirm that the interference was due to ethylene glycol or its metabolites, we performed a spiking experiment. Cross reactivity was linked to ethylene glycol and was low in our experiments (0.1-0.2%). Substantial amounts of ethylene glycol are required to slightly elevated GHB results, depending on the endogenous cutoff used. We can conclude that ethylene glycol can give rise to falsely elevated urinary GHB levels at ethylene glycol concentrations that are typically found in intoxications.

Prompt Diagnosis of Ethylene Glycol Intoxication by an Unusual "Lactate Gap": A Case Report.

IntroductionEthylene glycol intoxication can be lethal if diagnosis is delayed. Often, prompt diagnosis may need to be based on indirect laboratory findings.Case reportWe present a case of severe ethylene glycol intoxication whose diagnosis was based on an unusual “lactate gap.” The patient responded well to the treatment and had a full recovery.ConclusionA “lactate gap” can be helpful in establishing a diagnosis of ethylene glycol intoxication.

One-Week High-Dose β-Alanine Loading Improves World Tour Cyclists' Time-Trial Performance.

Supplementation with β-alanine is becoming a common practice in high-performance athletes. The purpose of the present study was to investigate the effects of a one-week high-dose β-alanine loading phase employing a sustained-release powder on preserving the time-trial performance capacity of world tour cyclists during overreaching training. Per day, 20 g of sustained-release β-alanine was administered during one week (7 days) of intensive team training camp in a randomised balanced placebo-controlled parallel trial design, with six participants in each β-alanine (BA) or placebo (PLA) group. A 10-min time trial (10′ TT) was carried out to analyse performance and biochemical variables. Anthropometry, paresthesia, and adverse event data were also collected. Power-based relative training load was quantified. Compared to placebo, the BA improved mean power (6.21%, 37.23 W; 95% CI: 3.98–70.48 W, p = 0.046), distance travelled (2.16%, p = 0.046) and total work (4.85%, p = 0.046) without differences in cadence (p = 0.506) or RPE. Lactate (p = 0.036) and anion gap (p = 0.047) were also higher in the BA group, without differences in pH or Bicarbonate. High daily and single doses were well tolerated. One-week high-dose β-alanine loading with a sustained-release powder blend can help attenuate 10′ TT performance losses of world tour cyclists due to intensive training.

Lactate Gap as Initial Indicator for Ethylene Glycol Toxicity

Lactate Gap as Initial Indicator for Ethylene Glycol Toxicity

Exercise training session-induced metabolic acidosis in barrel racing horses

ABSTRACT: In horses, acid-base balance disorders are common after intense exercise, with metabolic acidosis being the most common after high intensity and short duration exercise. Understanding the processes that cause them is fundamental for procedures, which aimed to improve the physical fitness of horses for athletic purposes, with fewer changes in homeostasis. The present study assessed the effect of barrel racing on acid base balance in Quarter Horse, at the following times: T0 - immediately before training; T1 - immediately after the end of the second course; T2 - one hour after the end of the second course. In T1, there was decrease (P<0.05) in the pH, HCO3 -, pCO2, cBase, tCO2 and strong ion difference concentrations, while the plasma lactate and anion gap increased (P<0.05). It was concluded that barrel racing training caused transient metabolic acidosis in the horses, and hyperlactatemia was still present after an hour of rest.

ARTERIAL VS SERUM LACTIC ACID DISCREPANCY

SESSION TITLE: Unusual Cases and Treatments in the ICU SESSION TYPE: Fellow Case Reports PRESENTED ON: 10/22/2019 3:45 PM - 4:45 PM INTRODUCTION: We are presenting a case where a significant difference was noticed between lactate levels measured by arterial blood gas (ABG) analyzer and serum chemistry analyzer; Lactate gap. Why does that happen? How does it help in supporting a diagnosis and monitoring a treatment? CASE PRESENTATION: A 46-year-old female was brought to the Emergency Department (ED) after her family called 911 for altered mental status and abnormal behavior. Emergency Medical Services personnel found the patient next to an empty bottle of Oxycodone/Acetaminophen and beer cans. In the ED, She was oriented only to person, unable to provide significant history regarding her medication/alcohol consumption. She denied homicidal or suicidal ideation. Few hours later, she progressively became more lethargic prompting intubation for airway protection. Physical exam was within normal limits except for the lethargy and tachypnea. Initial blood workup showed severe high anion gap metabolic acidosis, serum bicarbonate level of 5, anion gap of 24, calculated serum osmolality of 281, measured serum osmolality of 334, making an osmolal gap of 53. Serum lactate 1.2, Serum alcohol, acetone, salicylate and acetaminophen levels were undetectable. ABG, with lactate level, revealed a pH of 7.0, PaCO2 of 13, PaO2 of 151, bicarbonate of 3.2 and lactate of 20. Serial lactate discrepancies were noticed between measuring lactate by the ABG and the serum chemistry analyzers. Due to encephalopathy, high anion gap and osmolar gap, there was a high suspicion that she ingested methanol or ethylene glycol, so she was started on Sodium bicarbonate drip, fomepizole infusion and an emergent hemodialysis was initiated. After 1 session, her mental status improved and was extubated. Lactate gap, anion gap, osmolar gap and metabolic acidemia normalized. DISCUSSION: Ethylene glycol toxicity is known to cause a high anion gap and osmolal gap, especially early in presentation. The new thing to our knowledge, which was confirmed by published literature was that it may cause a lactate gap; a discrepancy between lactate levels measured by the ABG analyzer and the serum chemistry analyzer. This discrepancy is explained by the cross reactivity of the ABG analyzer with glycolate, a byproduct of ethylene glycol, resulting in high ABG lactate levels. This false positive result of lactate gap by the ABG analyzer can help to support the diagnosis of the ethylene glycol toxicity and monitor the treatment, that includes administration of Sodium bicarbonate to correct the severe academia, fomepizole to prevent conversion of ethylene glycol to the toxic metabolites and emergent dialysis to clear these metabolites before they cause acute tubular necrosis resulting in acute renal failure. CONCLUSIONS: Lactate gap noted through discrepancy between Lactate level on ABG and serum chemistry analyzers can be used to diagnose and monitor treatment for Ethylene Glycol toxicity. Reference #1: DOI:https://doi.org/10.1016/S0140-6736(01)06799-X DISCLOSURES: No relevant relationships by Moayyad Alziadat, source=Web Response No relevant relationships by Mohd Hazem Azzam, source=Web Response No relevant relationships by Anish Samuel, source=Web Response

“Please Mind the Gap”: The Lactate Gap as a Tool in Identifying Ethylene Glycol Toxicity

“Please Mind the Gap”: The Lactate Gap as a Tool in Identifying Ethylene Glycol Toxicity

Mind the Gap: Anion Gap, Osmolar Gap and Lactate Gap in Unresponsive Patient

Mind the Gap: Anion Gap, Osmolar Gap and Lactate Gap in Unresponsive Patient

Ethylene glycol poisoning and the lactate gap

Ethylene glycol poisoning and the lactate gap

Artifactual lactic acidosis from point of care analysis: mind the gap

A patient presented with severe acidosis, point-of-care (POC) lactate of 42 mmol/l. This led to suspicion of mesenteric ischemia and potential need for laparotomy. However, plasma lactates were <4 mmol/and ethylene glycol (EG) ingestion was subsequently diagnosed. We therefore wished to determine why discrepant lactates occur and whether this lactate gap (that is, the difference between lactate measured using two common methods) could be clinically useful.

The lactate gap revisited: variable interference with lactate analyses in ethylene glycol poisoning

(2010). The lactate gap revisited: variable interference with lactate analyses in ethylene glycol poisoning. British Journal of Biomedical Science: Vol. 67, No. 3, pp. 148-150.

Lactate gap and ethylene glycol poisoning

Lactate gap and ethylene glycol poisoning

Falsely elevated point-of-care lactate measurement after ingestion of ethylene glycol

A patient presented with severe acidosis and a point-of-care lactate measurement of 42 mmol/L. Mesenteric ischemia was suspected, with a potential need for laparotomy; however, plasma lactate measurements were below 4 mmol/L. Ethylene glycol ingestion was subsequently diagnosed. We therefore wished to determine why discrepancies in lactate measurements occur and whether this "lactate gap" could be clinically useful. We phlebotomized blood, added various concentrations of metabolites of ethylene glycol, and tested the resulting samples with the 5 most common lactate analyzers. With the Radiometer 700 point-of-care analyzer, glycolate addition resulted in an artifactual, massive lactate elevation, even at low glycolate concentrations. Another major ethylene glycol metabolite, glyoxylate (but not oxalate or formate), caused similar elevations. The i-STAT and Bayer point-of-care analyzers and the Beckman and Vitros laboratory analyzers reported minimal lactate elevations. Lactate gap was determined by comparing the Radiometer result with the corresponding result from any of the other analyzers. We demonstrated how inappropriate laparotomy or delayed therapy might occur if clinicians are unaware of this phenomenon or have access to only a single analyzer. We also showed that lactate gap can be exploited to expedite treatment, diagnose late ethylene-glycol ingestion and terminate dialysis. By comparing lactate results from the iSTAT or Bayer devices with that from the Radiometer, ethylene-glycol ingestion can be diagnosed at the point of care. This can expedite diagnosis and treatment by hours, compared with waiting for laboratory results for plasma ethylene glycol.

Acid-Base Balance during Continuous Veno-Venous Hemofiltration: The Impact of Severe Hepatic Failure

Continuous renal replacement therapy (CRRT) affects acid-base balance but the influence of severe hepatic failure (SHF) on this effect is unknown. To assess the effect of SHF on acid-base balance in patients receiving CVVH. Retrospective laboratory investigation. Forty patients with SHF and acute renal failure (ARF) treated with CVVH and 42 critically ill patients with severe ARF but no liver disease also treated with CVVH (controls). Retrieval of clinical and laboratory data from prospective unit and laboratory databases. Quantitative acid-base status assessment using the Stewart-Figge methodology. Comparison of findings between the two groups. Although CVVH had a major effect on acid base balance in both groups, patients with SHF had a higher mean lactate concentrations (4.8 vs. 3.1 mmol/L; p<0.0005), a greater base deficit compared to controls (-1 vs. 4.1 mEq/L; p<0.0001) and a lower PaCO 2 tension (36.8 vs. 42.5 mmHg; p<0.0001), despite the use of bicarbonate replacement fluid. The acidifying effect of hyperlactatemia was slightly worsened by an increased strong ion gap (9.3 vs. 4.9 mEq/L; p<0.0001). It was, however, attenuated by an increased strong ion difference apparent (SIDa) (43.6 vs. 41.9 mEq/L; p<0.05) secondary to hypochloremia (96 vs. 100 mmol/L; p<0.0001) and by hypoalbuminemia, although hypoalbuminemia in SHF patients (26 vs. 23; p<0.005) was less pronounced than in controls. The use of CVVH does not fully correct the independent acidifying effect of liver failure on acid-base status. Increased lactate and strong ion gap values maintain a persistent base deficit despite the alkalinizing effects of hypoalbuminemia and hypochloremia. The correction of acidosis in SHF patients may require more intensive CVVH.

Artifactual elevation of lactate in ethylene glycol poisoning

The diagnosis of ethylene glycol poisoning is based on nonspecific clinical symptoms and signs and indirect and direct laboratory measurement. Few institutions have timely access to direct measurement of ethylene glycol. As a result, diagnosis sometimes can be delayed and therapy initiated late. We present two cases of ethylene glycol poisoning. These cases demonstrate the need to recognize the false elevation of lactate in some chemistry analyzers due to the interference of glycolic acid, a metabolite of ethylene glycol. Using the “lactate gap” in comparing the measurement of lactate with two commonly used chemical analyzers aids in differentiating ethylene glycol poisoning from lactic acidosis.

Measuring the lactate gap

Combined elevations of anion and osmolar gaps are characteristic of methanol and ethylene glycol poisonings. However, the rapid diagnosis of ethylene glycol poisoning can be a challenge. We describe how an error in laboratory measurement can be used to identify a third gap, the lactate gap, which is highly suggestive of ethylene glycol poisoning and can speed the diagnosis of this potentially lethal condition.